Cholesterol will not mix with
water, and therefore, needs some assistance to travel throughout
the blood stream. With the help of a form of cholesterol HDL
(high density lipoprotein), packets of cholesterol are formed
to help move cholesterol through the blood. HDL helps
remove cholesterol from the body by transporting it to the liver.
Another form of cholesterol is LDL (low density lipoprotein).
LDL does not aid in the transportation of cholesterol
out of the body, instead it deposits cholesterol onto the vessel
wall. LDL molecules contain much more cholesterol than
HDL molecules.

How to Increase HDL

(Good Guys)

Exercise

Cessation of smoking

Weight reduction

How to Decrease LDL

(Bad Guys)

Decrease saturated fat intake

Maintain good body composition

Increase dietary fiber

Increase aerobic exercise

The total cholesterol/HDL ratio is more indicative
of cardiovascular disease than TC (total cholesterol).
The amount of HDL and LDL in the blood are added
together, this number for all practical purposes, indicates the
amount of total cholesterol. Therefore, if your HDL count
is low, the LDL count will account for the remainder of
the total. For men an acceptable ratio of TC/HDL
is 4.5 or below, and women is 4.0 or below.

Ratio of total Cholesterol to HDL

Risk

Men

Women

Very low (1/2 average)

<3.4

<3.3

Low risk

4.0

3.8

Average risk

5.0

4.5

Moderate risk (2x average)

9.5

7.0

High risk (3x risk)

>23

>11

Triglycerides (mg/dl)

< 130

Desirable

< 150

Normal

150-199

Borderline

200-499

High

>= 500

Very High

Ratio of LDL to HDL

Risk

Men

Women

Very low (1/2 average)

1

1.5

Average risk

3.6

3.2

Moderate risk (2x average)

6.3

5.0

High risk (3x risk)

8

6.1

HDL levels have an inverse relationship with coronary
heart disease. The ability of HDL to predict the development
of coronary atherosclerosis has been estimated to be four times
greater than LDL and eight times greater than TC.
Treatment is recommended for those with an HDL level below
40 mg/dL. An HDL of 60 mg/dL is considered protection
against heart disease.

New MNR imaging tests assess the size of LDL particles.
Small LDL particles are associated with a higher risk
of cardiovascular disease.

Triglycerides

Elevated triglycerides in the blood increase the risk of heart
disease. Triglycerides do not come directly from dietary fats.
Instead, they are produced in the liver from any excess carbohydrates
that have not been used for energy.

NCEP Blood Lipid Guidelines

Adults 20 years and older should undergo cholesterol screening
(total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides)
every 5 years. Blood samples should be obtained after fasting.

LDL Cholesterol (mg/dl)

<100

Optimal

100-129

Near Optimal

130-159

Borderline High

160-189

High

> 190

Very High

Total Cholesterol (mg/dl)

<200

Desirable

200-239

Borderline

>=240

High risk

HDL Cholesterol (mg/dl)

<40

Low (undesirable

>60

High (desirable)

Triglycerides (mg/dl)

<150

Normal

150-199

Borderline High

200-499

High

>500

Very High

The National Cholesterol Education Program (May 16, 2001),
Journal of the American Medical Association

Blood Lipid Transport

After
consuming a meal containing fat, the blood undergoes a transient
increase in lipids, particularly triacylglycerols, lasting several
hours. This is known as postprandial lipemia. Individuals consuming
a typical Western diet spend approximately 18 hours per day in
this state.

Exogenous fat transport begins in the intestine where dietary
fats are packaged into lipoprotein particles called chylomicrons.
Chylomicrons enter the bloodstream and deliver their triglyceride
to adipose tissue and muscle. The remnant of chylomicrons is
removed from the circulation by the liver.

Endogenous fat transportation begins when the liver secretes
a Very Low Density Lipoprotein particle (VLDL). When a VLDL particle
reaches the capillary of muscle or adipose tissue, its triglyceride
is extracted, leaving an Intermediate Density Lipoprotein (IDL).
Half of the IDL particles are removed from circulation by the
liver within two to six hours of their formation. The remaining
IDL transforms into Low Density Lipoproteins (LDL) which circulate
for approximately two and a half days before binding to LDL receptors
in the liver and other tissues.

Small dense low density lipoprotein (LDL) are more atherogenic
that larger LDL particles because they are

more easily enter the vessel wall

more prone to oxidative modification

bind more tightly to the arterial wall

cleared more slowly

The composition of triglyceride-rich lipoproteins (TRLs) are
metabolically linked to LDL. LDL particle size is primarily affected
by the plasma TG levels. Postprandial hyperlipidemia is associated
with an increase in the proportion of small, dense LDL. Furthermore,
prolonged lipemia promotes the transfer of core lipids between
TRLs and high density lipoprotein (HDL) leading to a reduction
in HDL cholesterol levels. This combination is known as the lipid
triad or atherogenic lipoprotein profile:

Cholesterol Regulation

Elevated circulating cholesterol reduces the cells ability
to make its own cholesterol by turning off the production of
HMG CoA reductase, which interrupts a step in the biosynthetic
pathway of cholesterol. Incoming LDL derived cholesterol promotes
the storage of cholesterol in the cell by activating ACAT which
reattaches a fatty acid to excess cholesterol molecules. This
results in cholesterol esters that are deposited in storage droplets.
The accumulation of cholesterol within the cell drives a feedback
mechanism which stops the cells synthesis of new LDL receptors.
The cell adjusts its receptors, so only enough cholesterol is
brought in to supply its needs.

With Familial Hypercholesterolemia, an inherited mutant gene
causes the absence of LDL receptors. High circulating levels
of LDL are found to be caused by an increased production and
a decrease in the removal of LDL. Consequently, Familial Hypercholesterolemia
leads to high blood cholesterol and heart attacks in the young.